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[PMID]:28450394
[Au] Autor:Korge P; John SA; Calmettes G; Weiss JN
[Ad] Endereço:From the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
[Ti] Título:Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex II.
[So] Source:J Biol Chem;292(24):9896-9905, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Succinate-driven reverse electron transport (RET) through complex I is hypothesized to be a major source of reactive oxygen species (ROS) that induces permeability transition pore (PTP) opening and damages the heart during ischemia/reperfusion. Because RET can only generate ROS when mitochondria are fully polarized, this mechanism is self-limiting once PTP opens during reperfusion. In the accompanying article (Korge, P., Calmettes, G., John, S. A., and Weiss, J. N. (2017) 292, 9882-9895), we showed that ROS production after PTP opening can be sustained when complex III is damaged (simulated by antimycin). Here we show that complex II can also contribute to sustained ROS production in isolated rabbit cardiac mitochondria following inner membrane pore formation induced by either alamethicin or calcium-induced PTP opening. Two conditions are required to maximize malonate-sensitive ROS production by complex II in isolated mitochondria: ( ) complex II inhibition by atpenin A5 or complex III inhibition by stigmatellin that results in succinate-dependent reduction of the dicarboxylate-binding site of complex II (site II ); ( ) pore opening in the inner membrane resulting in rapid efflux of succinate/fumarate and other dicarboxylates capable of competitively binding to site II The decrease in matrix [dicarboxylate] allows O access to reduced site II , thereby making electron donation to O possible, explaining the rapid increase in ROS production provided that site II is reduced. Because ischemia is known to inhibit complexes II and III and increase matrix succinate/fumarate levels, we hypothesize that by allowing dicarboxylate efflux from the matrix, PTP opening during reperfusion may activate sustained ROS production by this mechanism after RET-driven ROS production has ceased.
[Mh] Termos MeSH primário: Complexo II de Transporte de Elétrons/metabolismo
Mitocôndrias Cardíacas/metabolismo
Modelos Moleculares
Espécies Reativas de Oxigênio/agonistas
[Mh] Termos MeSH secundário: Alameticina/farmacologia
Animais
Sítios de Ligação
Ligação Competitiva
Biocatálise/efeitos dos fármacos
Sinalização do Cálcio/efeitos dos fármacos
Transporte de Elétrons/efeitos dos fármacos
Complexo II de Transporte de Elétrons/antagonistas & inibidores
Complexo II de Transporte de Elétrons/química
Inibidores Enzimáticos/farmacologia
Fumaratos/metabolismo
Ionóforos/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias Cardíacas/química
Mitocôndrias Cardíacas/efeitos dos fármacos
Oxirredução
Permeabilidade/efeitos dos fármacos
Polienos/farmacologia
Porosidade
Piridonas/farmacologia
Coelhos
Espécies Reativas de Oxigênio/metabolismo
Ácido Succínico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Fumarates); 0 (Ionophores); 0 (Polyenes); 0 (Pyridones); 0 (Reactive Oxygen Species); 119509-24-9 (atpenin A5); 27061-78-5 (Alamethicin); 91682-96-1 (stigmatellin); AB6MNQ6J6L (Succinic Acid); EC 1.3.5.1 (Electron Transport Complex II)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.768325


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[PMID]:27773804
[Au] Autor:Hung MJ; Kao YC; Mao CT; Chen TH; Chen WS
[Ad] Endereço:Section of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Keelung City, Taiwan. Electronic address: hmj1447@cgmh.org.tw.
[Ti] Título:Aliskiren attenuates the effects of interleukin-6 on endothelial nitric oxide synthase and caveolin-1 in human aortic endothelial cells.
[So] Source:Nitric Oxide;61:45-54, 2016 Dec 30.
[Is] ISSN:1089-8611
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renin inhibitors enhance endothelial nitric oxide synthase (eNOS) bioavailability and have protective effects on endothelial function and atherosclerotic changes. This study was designed to investigate whether aliskiren attenuates the effects of interleukin-6 (IL-6) on eNOS and the eNOS-caveolin-1 interaction in human aortic endothelial cells (HAECs). In this study, we examined the effects of pretreatment with aliskiren on the changes of IL-6-induced expression and activation of eNOS and caveolin-1 in cultured HAECs. IL-6 inhibited and aliskiren increased the phosphorylation of eNOS at Ser1177; however, eNOS protein and mRNA expression were not changed. Pretreatment with aliskiren attenuated the inhibitory effects of IL-6 on eNOS phosphorylation and nitric oxide production. IL-6 increased the phosphorylation of caveolin-1 at Tyr14 without affecting the caveolin-1 protein and mRNA expression. Pretreatment with aliskiren attenuated the effects of IL-6 on caveolin-1 phosphorylation. The binding of eNOS and caveolin-1, as determined by a co-immunoprecipitation assay, was increased by IL-6 treatment and decreased by aliskiren pretreatment. Furthermore, treatment with short interfering RNA of the extracellular signal-regulated kinase gene reversed the effects of IL-6 and aliskiren on eNOS and caveolin-1. In conclusion, aliskiren attenuates the inhibitory effects of IL-6 on eNOS phosphorylation and nitric oxide production and IL-6 induced caveolin-1 phosphorylation. In addition, aliskiren reverses the effects of IL-6 on the eNOS-caveolin-1 interaction.
[Mh] Termos MeSH primário: Amidas/farmacologia
Aorta/citologia
Caveolina 1/metabolismo
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Fumaratos/farmacologia
Óxido Nítrico Sintase Tipo III/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (CAV1 protein, human); 0 (Caveolin 1); 0 (Fumarates); 502FWN4Q32 (aliskiren); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29173237
[Au] Autor:Robertson RC; Seira Oriach C; Murphy K; Moloney GM; Cryan JF; Dinan TG; Ross RP; Stanton C
[Ad] Endereço:1School of Microbiology,University College Cork,Cork,Republic of Ireland.
[Ti] Título:Deficiency of essential dietary n-3 PUFA disrupts the caecal microbiome and metabolome in mice.
[So] Source:Br J Nutr;118(11):959-970, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:n-3 PUFA are lipids that play crucial roles in immune-regulation, cardio-protection and neurodevelopment. However, little is known about the role that these essential dietary fats play in modulating caecal microbiota composition and the subsequent production of functional metabolites. To investigate this, female C57BL/6 mice were assigned to one of three diets (control (CON), n-3 supplemented (n3+) or n-3 deficient (n3-)) during gestation, following which their male offspring were continued on the same diets for 12 weeks. Caecal content of mothers and offspring were collected for 16S sequencing and metabolic phenotyping. n3- male offspring displayed significantly less % fat mass than n3+ and CON. n-3 Status also induced a number of changes to gut microbiota composition such that n3- offspring had greater abundance of Tenericutes, Anaeroplasma and Coriobacteriaceae. Metabolomics analysis revealed an increase in caecal metabolites involved in energy metabolism in n3+ including α-ketoglutaric acid, malic acid and fumaric acid. n3- animals displayed significantly reduced acetate, butyrate and total caecal SCFA production. These results demonstrate that dietary n-3 PUFA regulate gut microbiota homoeostasis whereby n-3 deficiency may induce a state of disturbance. Further studies are warranted to examine whether these microbial and metabolic disturbances are causally related to changes in metabolic health outcomes.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos da Nutrição Animal
Ceco/microbiologia
Ácidos Graxos Ômega-3/deficiência
Microbioma Gastrointestinal
[Mh] Termos MeSH secundário: Animais
Composição Corporal
DNA Bacteriano/isolamento & purificação
Dieta
Suplementos Nutricionais
Ácidos Graxos/metabolismo
Ácidos Graxos Ômega-3/sangue
Feminino
Fumaratos/metabolismo
Ácidos Cetoglutáricos/metabolismo
Malatos/metabolismo
Masculino
Metaboloma
Metabolômica
Camundongos
Camundongos Endogâmicos C57BL
RNA Ribossômico 16S/isolamento & purificação
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (Fatty Acids); 0 (Fatty Acids, Omega-3); 0 (Fumarates); 0 (Ketoglutaric Acids); 0 (Malates); 0 (RNA, Ribosomal, 16S); 817L1N4CKP (malic acid); 88XHZ13131 (fumaric acid); 8ID597Z82X (alpha-ketoglutaric acid)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002999


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[PMID]:29018174
[Au] Autor:Kristensen SL; Jhund PS; Mogensen UM; Rørth R; Abraham WT; Desai A; Dickstein K; Rouleau JL; Zile MR; Swedberg K; Packer M; Solomon SD; Køber L; McMurray JJV; PARADIGM-HF and ATMOSPHERE Committees and Investigators
[Ad] Endereço:From the BHF Cardiovascular Research Centre, University of Glasgow, United Kingdom (S.L.K., P.S.J., U.M.M., R.R., J.J.V.M.); Department of Cardiology, Rigshospitalet University Hospital, Copenhagen, Denmark (S.L.K., U.M.M., R.R., L.K.); The Division of Cardiovascular Medicine, Davis Heart and Lung R
[Ti] Título:Prognostic Value of N-Terminal Pro-B-Type Natriuretic Peptide Levels in Heart Failure Patients With and Without Atrial Fibrillation.
[So] Source:Circ Heart Fail;10(10), 2017 Oct.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with heart failure (HF) and atrial fibrillation (AF) have higher circulating levels of NT-proBNP (N-terminal pro-B-type natriuretic peptide) than HF patients without AF. There is uncertainty about the prognostic importance of a given concentration of NT-proBNP in HF patients with and without AF. We investigated this question in a large cohort of patients with HF and reduced ejection fraction. METHODS AND RESULTS: We studied 14 737 patients with HF and reduced ejection fraction and a measurement of NT-proBNP at time of screening, enrolled in either the PARADIGM-HF trial (Prospective Comparison of ARNI With ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure) or the ATMOSPHERE trial (Aliskiren Trial to Minimize Outcomes in Patients With Heart Failure), of whom 3575 (24%) had AF on their baseline ECG. Median (Q1, Q3) levels of NT-proBNP were 1817 pg/mL (1095-3266 pg/mL) in those with AF and 1271 pg/mL (703-2569 pg/mL) in those without ( <0.0001). Patients with AF were older (67 versus 62 years), had worse New York Heart Association class (III/IV; 36% versus 24%), and experienced fewer previous HF hospitalizations (52% versus 61%) or myocardial infarction (30% versus 46%); all <0.001. We categorized patients with and without AF into 5 NT-proBNP bands: <400, 400 to 999 (reference), 1000 to 1999, 2000 to 2999, and ≥3000 pg/mL. For the primary composite outcome of cardiovascular death or HF hospitalization, event rates differed for patients with and without AF in the lowest band (<400 pg/mL; 8.2 versus 5.0 per 100 patient-years), but not for the higher bands (400-999 pg/mL, 7.4 versus 7.7 per 100 patient-years; 1000-1999 pg/mL, 9.8 versus 11.4 per 100 patient-year; 2000-2999 pg/mL, 13.5 versus 13.4 per 100 patient-years; ≥3000 pg/mL, 22.7 versus 23.0 per 100 patient-years). These findings were consistent whether NT-proBNP was examined as a categorical or continuous variable and before and after adjustment for other prognostic variables. We found similar results for the components of the composite outcome and all-cause mortality. CONCLUSIONS: HF and reduced ejection fraction patients with AF had higher NT-proBNP than those without AF. However, above a concentration of 400 pg/mL (representing most patients in each group), NT-proBNP had similar predictive value for adverse cardiovascular outcomes, irrespective of AF status. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier NCT00853658 (ATMOSPHERE) and NCT01035255 (PARADIGM-HF).
[Mh] Termos MeSH primário: Fibrilação Atrial/sangue
Doenças Cardiovasculares/mortalidade
Insuficiência Cardíaca/sangue
Hospitalização/estatística & dados numéricos
Peptídeo Natriurético Encefálico/sangue
Fragmentos de Peptídeos/sangue
[Mh] Termos MeSH secundário: Idoso
Amidas/uso terapêutico
Aminobutiratos/uso terapêutico
Antagonistas de Receptores de Angiotensina/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Fibrilação Atrial/complicações
Estudos de Casos e Controles
Estudos de Coortes
Enalapril/uso terapêutico
Feminino
Fumaratos/uso terapêutico
Insuficiência Cardíaca/complicações
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Volume Sistólico
Tetrazóis/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Aminobutyrates); 0 (Angiotensin Receptor Antagonists); 0 (Antihypertensive Agents); 0 (Fumarates); 0 (LCZ 696); 0 (Peptide Fragments); 0 (Tetrazoles); 0 (pro-brain natriuretic peptide (1-76)); 114471-18-0 (Natriuretic Peptide, Brain); 502FWN4Q32 (aliskiren); 69PN84IO1A (Enalapril)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE


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[PMID]:28847082
[Au] Autor:Liu H; Zhao S; Jin Y; Yue X; Deng L; Wang F; Tan T
[Ad] Endereço:Beijing Bioprocess Key Laboratory, State Key Laboratory of Chemical Resource Engineering, Beijing University of Chemical Technology, Beijing 100029, PR China.
[Ti] Título:Production of fumaric acid by immobilized Rhizopus arrhizus RH 7-13-9# on loofah fiber in a stirred-tank reactor.
[So] Source:Bioresour Technol;244(Pt 1):929-933, 2017 Nov.
[Is] ISSN:1873-2976
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fumaric acid is an important building-block chemical. The production of fumaric acid by fermentation is possible. Loofah fiber is a natural, biodegradable, renewable polymer material with highly sophisticated and pore structure. This work investigated a new immobilization method using loofah fiber as carrier to produce fumaric acid in a stirred-tank reactor. Compared with other carriers, loofah fiber was proven to be efficiently and successfully used in the reactor. After the optimization process, 20g addition of loofah fiber and 400rpm agitation speed were chosen as the most suitable process conditions. 30.3g/L fumaric acid in the broth as well as 19.16g fumaric acid in the precipitation of solid was achieved, while the yield from glucose reached 0.211g/g. Three batches of fermentation using the same loofah fiber carrier were conducted successfully, which meant it provided a new method to produce fumaric acid in a stirred-tank reactor.
[Mh] Termos MeSH primário: Fumaratos
Rhizopus
[Mh] Termos MeSH secundário: Reatores Biológicos
Fermentação
Luffa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fumarates); 88XHZ13131 (fumaric acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE


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[PMID]:28753620
[Au] Autor:Chung S; Kim S; Kim M; Koh ES; Shin SJ; Park CW; Chang YS; Kim HS
[Ad] Endereço:Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
[Ti] Título:Treatment combining aliskiren with paricalcitol is effective against progressive renal tubulointerstitial fibrosis via dual blockade of intrarenal renin.
[So] Source:PLoS One;12(7):e0181757, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to assess any potential additive effects of a treatment combining aliskiren with paricalcitol on reducing renal fibrosis. C57BL/6J mice were treated individually with aliskiren and/or paricalcitol until 7 days after initiation of unilateral ureteral obstruction (UUO).In obstructed kidneys of UUO mice, monotherapy with aliskiren or paricalcitol significantly attenuated interstitial fibrosis, collagen IV accumulation, and α-smooth muscle actin- and terminal deoxynucleotidyl transferase-mediated biotin nick end-labeling-positive cells. The combination treatment showed additive efficacy in inhibition of these parameters. Renal NADPH oxidase (Nox)1 and Nox2 were significantly decreased by aliskiren or paricalcitol alone or in combination, while renal Nox4 expression was significantly reduced by paricalcitol mono- or combination treatment. Increased levels of p-Erk and p-p38 MAPK, and NF-κB in UUO kidneys were also significantly reduced by either aliskiren or paricalcitol treatment alone or in combination. Aliskiren or paricalcitol monotherapy significantly reduced the expression of (pro)renin receptor in UUO kidneys. In addition, aliskiren tended to augment renin expression in UUO kidneys, but paricalcitol reduced its expression level. The combination treatment effectively blocked both (pro)renin receptor and renin expression induced by aliskiren, and resulted in a further reduction of the renal expression of angiotensin II AT1 receptor. Aliskiren failed to increase the expression of vitamin D receptor in UUO kidneys, but the combination treatment restored its expression level. Taken together, a treatment combining aliskiren with paricalcitol better inhibits UUO-induced renal injury. The mechanism of this synergy may involve more profound inhibition of the intrarenal renin-angiotensin system.
[Mh] Termos MeSH primário: Amidas/uso terapêutico
Progressão da Doença
Ergocalciferóis/uso terapêutico
Fumaratos/uso terapêutico
Nefropatias/tratamento farmacológico
Rim/metabolismo
Renina/metabolismo
[Mh] Termos MeSH secundário: Amidas/farmacologia
Animais
Apoptose/efeitos dos fármacos
Colágeno Tipo IV/metabolismo
Quimioterapia Combinada
Ergocalciferóis/farmacologia
Fibrose
Fumaratos/farmacologia
Mediadores da Inflamação/metabolismo
Nefropatias/patologia
Masculino
Camundongos Endogâmicos C57BL
Miofibroblastos/efeitos dos fármacos
Miofibroblastos/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Receptores de Calcitriol/metabolismo
Sistema Renina-Angiotensina/efeitos dos fármacos
Resultado do Tratamento
Obstrução Ureteral/tratamento farmacológico
Obstrução Ureteral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Collagen Type IV); 0 (Ergocalciferols); 0 (Fumarates); 0 (Inflammation Mediators); 0 (Receptors, Calcitriol); 502FWN4Q32 (aliskiren); 6702D36OG5 (paricalcitol); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181757


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[PMID]:28724547
[Au] Autor:Okada Y; Shibata S; Fujimoto N; Best SA; Levine BD; Fu Q
[Ad] Endereço:Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Dallas, Texas.
[Ti] Título:Long-term effects of a renin inhibitor versus a thiazide diuretic on arterial stiffness and left ventricular diastolic function in elderly hypertensive patients.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R400-R409, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arterial stiffness and cardiac function are important predictors of cardiovascular events in patients with hypertension, even with adequate blood pressure (BP) control. We evaluated whether a direct renin inhibitor, aliskiren, reduces arterial stiffness and modulates left ventricular function compared with a diuretic, hydrochlorothiazide, in elderly hypertensive patients. Twenty-one hypertensive patients [67 ± 14 (SD) yr] were randomly assigned to receive 6-mo aliskiren ( = 11) or hydrochlorothiazide ( = 10)-based therapy. We assessed ß-stiffness of the local arteries, arterial elastance ( ), and echocardiographic variables, including early ( ) and late ( ) mitral inflow velocity, deceleration time of E, early ( ') and late ( ') diastolic mitral annular velocity, and left ventricular end-systolic elastance ( ) before and after treatment. BP decreased similarly ( < 0.001) after both therapies. ß-Stiffness of the carotid artery decreased after aliskiren but increased after hydrochlorothiazide treatment (aliskiren: 6.42 ± 2.34 pre vs. 5.07 ± 1.29 post; hydrochlorothiazide: 5.05 ± 1.78 vs. 7.25 ± 2.68, = 0.001 for interaction). ß-Stiffness of the femoral and radial arteries were not different after either treatment. Different from aliskiren, decreased (73 ± 16 vs. 67 ± 14 cm/s, = 0.026), and the deceleration time was prolonged (218 ± 40 vs. 236 ± 35 ms, = 0.032) after hydrochlorothiazide therapy, whereas the / , and ' remained unchanged after both treatments. and decreased after aliskiren therapy (both < 0.05), whereas the / (ventricular-arterial coupling) was maintained after both treatments. Thus, aliskiren decreased the stiffness of carotid artery and left ventricular end-systolic elastance with maintenance of ventricular-arterial coupling without any effects on diastolic filling, while hydrochlorothiazide increased carotid arterial stiffness and slowed early diastolic filling in elderly hypertensive patients.
[Mh] Termos MeSH primário: Amidas/farmacologia
Diástole/efeitos dos fármacos
Fumaratos/farmacologia
Hidroclorotiazida/farmacologia
Hipertensão/tratamento farmacológico
Renina/antagonistas & inibidores
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
Rigidez Vascular/efeitos dos fármacos
Função Ventricular Esquerda/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Amidas/uso terapêutico
Anti-Hipertensivos/farmacologia
Anti-Hipertensivos/uso terapêutico
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Diástole/fisiologia
Ecocardiografia
Feminino
Artéria Femoral/efeitos dos fármacos
Artéria Femoral/fisiopatologia
Fumaratos/uso terapêutico
Seres Humanos
Hidroclorotiazida/uso terapêutico
Hipertensão/diagnóstico por imagem
Hipertensão/fisiopatologia
Masculino
Meia-Idade
Artéria Radial/efeitos dos fármacos
Artéria Radial/fisiopatologia
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
Resultado do Tratamento
Rigidez Vascular/fisiologia
Função Ventricular Esquerda/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Amides); 0 (Antihypertensive Agents); 0 (Fumarates); 0 (Sodium Chloride Symporter Inhibitors); 0J48LPH2TH (Hydrochlorothiazide); 502FWN4Q32 (aliskiren); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00125.2017


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[PMID]:28715411
[Au] Autor:Fyson N; King J; Belcher T; Preston A; Colijn C
[Ad] Endereço:Department of Mathematics, Imperial College, London, UK.
[Ti] Título:A curated genome-scale metabolic model of Bordetella pertussis metabolism.
[So] Source:PLoS Comput Biol;13(7):e1005639, 2017 Jul.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Gram-negative bacterium Bordetella pertussis is the causative agent of whooping cough, a serious respiratory infection causing hundreds of thousands of deaths annually worldwide. There are effective vaccines, but their production requires growing large quantities of B. pertussis. Unfortunately, B. pertussis has relatively slow growth in culture, with low biomass yields and variable growth characteristics. B. pertussis also requires a relatively expensive growth medium. We present a new, curated flux balance analysis-based model of B. pertussis metabolism. We enhance the model with an experimentally-determined biomass objective function, and we perform extensive manual curation. We test the model's predictions with a genome-wide screen for essential genes using a transposon-directed insertional sequencing (TraDIS) approach. We test its predictions of growth for different carbon sources in the medium. The model predicts essentiality with an accuracy of 83% and correctly predicts improvements in growth under increased glutamate:fumarate ratios. We provide the model in SBML format, along with gene essentiality predictions.
[Mh] Termos MeSH primário: Bordetella pertussis/genética
Bordetella pertussis/metabolismo
Genoma Bacteriano/genética
Modelos Biológicos
[Mh] Termos MeSH secundário: Fumaratos/metabolismo
Ácido Glutâmico/metabolismo
Seres Humanos
Análise do Fluxo Metabólico
Curva ROC
Coqueluche/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fumarates); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005639


  9 / 3787 MEDLINE  
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[PMID]:28700686
[Au] Autor:Chou CL; Lin H; Chen JS; Fang TC
[Ad] Endereço:Division of Nephrology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
[Ti] Título:Renin inhibition improves metabolic syndrome, and reduces angiotensin II levels and oxidative stress in visceral fat tissues in fructose-fed rats.
[So] Source:PLoS One;12(7):e0180712, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renin-angiotensin system in visceral fat plays a crucial role in the pathogenesis of metabolic syndrome in fructose-fed rats. However, the effects of renin inhibition on visceral adiposity in metabolic syndrome are not fully investigated. We investigated the effects of renin inhibition on visceral adiposity in fructose-fed rats. Male Wistar-Kyoto rats were divided into 4 groups for 8-week experiments: Group Con (standard chow diet), Group Fru (high-fructose diet; 60% fructose), Group FruA (high-fructose diet and concurrent aliskiren treatment; 100 mg/kg body weight [BW] per day), and Group FruB (high-fructose diet and subsequent, i.e. 4 weeks after initiating high-fructose feeding, aliskiren treatment; 100 mg/kg BW per day). The high-fructose diet induced metabolic syndrome, increased visceral fat weights and adipocyte sizes, and augmented angiotensin II (Ang II), NADPH oxidase (NOX) isoforms expressions, oxidative stress, and dysregulated production of adipocytokines from visceral adipose tissues. Concurrent and subsequent aliskiren administration ameliorated metabolic syndrome, dysregulated adipocytokines, and visceral adiposity in high fructose-fed hypertensive rats, and was associated with reducing Ang II levels, NOX isoforms expressions and oxidative stress in visceral fat tissues. Therefore, this study demonstrates renin inhibition could improve metabolic syndrome, and reduce Ang II levels and oxidative stress in visceral fat tissue in fructose-fed rats, and suggests that visceral adipose Ang II plays a crucial role in the pathogenesis of metabolic syndrome in fructose-fed rats.
[Mh] Termos MeSH primário: Angiotensina II/metabolismo
Comportamento Alimentar
Gordura Intra-Abdominal/metabolismo
Gordura Intra-Abdominal/patologia
Síndrome Metabólica/tratamento farmacológico
Estresse Oxidativo
Renina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Adipócitos/patologia
Adipocinas/sangue
Amidas/farmacologia
Amidas/uso terapêutico
Animais
Glicemia/metabolismo
Pressão Sanguínea/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Colesterol/sangue
Frutose
Fumaratos/farmacologia
Fumaratos/uso terapêutico
Insulina/sangue
Masculino
Síndrome Metabólica/sangue
Síndrome Metabólica/fisiopatologia
Estresse Oxidativo/efeitos dos fármacos
Ratos Endogâmicos WKY
Renina/metabolismo
Superóxido Dismutase/metabolismo
Sístole/efeitos dos fármacos
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adipokines); 0 (Amides); 0 (Blood Glucose); 0 (Fumarates); 0 (Insulin); 0 (Thiobarbituric Acid Reactive Substances); 0 (Triglycerides); 11128-99-7 (Angiotensin II); 30237-26-4 (Fructose); 502FWN4Q32 (aliskiren); 97C5T2UQ7J (Cholesterol); EC 1.15.1.1 (Superoxide Dismutase); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180712


  10 / 3787 MEDLINE  
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[PMID]:28674067
[Au] Autor:Chan CH; Levar CE; Jiménez-Otero F; Bond DR
[Ad] Endereço:BioTechnology Institute, University of Minnesota-Twin Cities, St. Paul, Minnesota, USA.
[Ti] Título:Genome Scale Mutational Analysis of Geobacter sulfurreducens Reveals Distinct Molecular Mechanisms for Respiration and Sensing of Poised Electrodes versus Fe(III) Oxides.
[So] Source:J Bacteriol;199(19), 2017 Oct 01.
[Is] ISSN:1098-5530
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:generates electrical current by coupling intracellular oxidation of organic acids to the reduction of proteins on the cell surface that are able to interface with electrodes. This ability is attributed to the bacterium's capacity to respire other extracellular electron acceptors that require contact, such as insoluble metal oxides. To directly investigate the genetic basis of electrode-based respiration, we constructed transposon-insertion sequencing (Tn-Seq) libraries for growth, with soluble fumarate or an electrode as the electron acceptor. Libraries with >33,000 unique insertions and an average of 9 insertions/kb allowed an assessment of each gene's fitness in a single experiment. Mutations in 1,214 different genomic features impaired growth with fumarate, and the significance of 270 genes unresolved by annotation due to the presence of one or more functional homologs was determined. Tn-Seq analysis of -0.1 V versus standard hydrogen electrode (SHE) electrode-grown cells identified mutations in a subset of genes encoding cytochromes, processing systems for proline-rich proteins, sensory networks, extracellular structures, polysaccharides, and metabolic enzymes that caused at least a 50% reduction in apparent growth rate. Scarless deletion mutants of select genes identified via Tn-Seq revealed a new putative porin-cytochrome conduit complex ( ) crucial for growth with electrodes, which was not required for Fe(III) oxide reduction. In addition, four mutants lacking components of a putative methyl-accepting chemotaxis-cyclic dinucleotide sensing network ( ) were defective in electrode colonization but grew normally with Fe(III) oxides. These results suggest that possesses distinct mechanisms for recognition, colonization, and reduction of electrodes compared to Fe(III) oxides. Since metal oxide electron acceptors are insoluble, one hypothesis is that cells sense and reduce metals using the same molecular mechanisms used to form biofilms on electrodes and produce electricity. However, by simultaneously comparing thousands of transposon mutants undergoing electrode-dependent respiration, we discovered new cytochromes and chemosensory proteins supporting growth with electrodes that are not required for metal respiration. This supports an emerging model where recognizes surfaces and forms conductive biofilms using mechanisms distinct from those used for growth with metal oxides. These findings provide a possible explanation for studies that correlate electricity generation with syntrophic interspecies electron transfer by and reveal many previously unrecognized targets for engineering this useful capability in other organisms.
[Mh] Termos MeSH primário: Compostos Férricos/metabolismo
Genoma Bacteriano
Geobacter/genética
Geobacter/metabolismo
Mutação
[Mh] Termos MeSH secundário: Proteínas de Bactérias/metabolismo
Biofilmes/crescimento & desenvolvimento
Elementos de DNA Transponíveis
Eletrodos
Transporte de Elétrons
Fumaratos/metabolismo
Fumaratos/farmacologia
Biblioteca Genômica
Geobacter/efeitos dos fármacos
Geobacter/crescimento & desenvolvimento
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (DNA Transposable Elements); 0 (Ferric Compounds); 0 (Fumarates); 1K09F3G675 (ferric oxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE



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